The objective of this Molecular Biology Core is to provide Core members with molecular biology tools to pursue Superfund-related research. Our member's research is focused on studying the toxicity and carcinogenicity induced by Superfund-related metals and polycyclic aromatic hydrocarbons (PAH), the genetic and epigenetic factors in determining an individual's susceptibility to these toxicants, and genes and gene products involved in the metabolism of Superfund toxicants. This Core aims to establish molecular techniques and expertise necessary for this research. Thus far, we have developed methods to determine the epigenetic changes at the sequence level in the p53 gene, and to map and quantify metal and PAH-DNA damage at both defined fragment and single-nucleotide resolution. These two approaches involve the use of state-of-the-art technology: ligation-mediated PCR (LMPCR) and DNA sequencing. For mapping epigenetic state-of-the-art technology: ligation-mediated PCR (LMPCR) and needed to execute these sophisticated experiments are also laborious and require extensive training. The reagents (UvrABC nucleases) used in these approaches also require laborious and extensive preparation. Furthermore, the results obtained from these experiments would be best interpreted by trained, experienced researchers. The Molecular Biology Core will centralize both equipment and expertise to provide this highly specialized service to all researchers involved in this proposal, with the possibility to provide service nationwide if necessary.

Agency
National Institute of Health (NIH)
Institute
National Institute of Environmental Health Sciences (NIEHS)
Type
Hazardous Substances Basic Research Grants Program (NIEHS) (P42)
Project #
1P42ES010344-01
Application #
6335594
Study Section
Special Emphasis Panel (ZES1-MAO-A (G2))
Project Start
2000-06-01
Project End
2005-03-31
Budget Start
Budget End
Support Year
1
Fiscal Year
2000
Total Cost
$164,076
Indirect Cost
Name
New York University
Department
Type
DUNS #
City
New York
State
NY
Country
United States
Zip Code
10016
Niu, Yingmei; DesMarais, Thomas L; Tong, Zhaohui et al. (2015) Oxidative stress alters global histone modification and DNA methylation. Free Radic Biol Med 82:22-8
Brocato, Jason; Hernandez, Michelle; Laulicht, Freda et al. (2015) In Vivo Exposures to Particulate Matter Collected from Saudi Arabia or Nickel Chloride Display Similar Dysregulation of Metabolic Syndrome Genes. J Toxicol Environ Health A 78:1421-36
Brocato, Jason; Chen, Danqi; Liu, Jianli et al. (2015) A Potential New Mechanism of Arsenic Carcinogenesis: Depletion of Stem-Loop Binding Protein and Increase in Polyadenylated Canonical Histone H3.1 mRNA. Biol Trace Elem Res 166:72-81
Brocato, Jason; Costa, Max (2015) SATB1 and 2 in colorectal cancer. Carcinogenesis 36:186-91
Brocato, Jason; Wu, Fen; Chen, Yu et al. (2015) Association between sleeping hours and cardiometabolic risk factors for metabolic syndrome in a Saudi Arabian population. BMJ Open 5:e008590
Brocato, Jason; Chervona, Yana; Costa, Max (2014) Molecular responses to hypoxia-inducible factor 1? and beyond. Mol Pharmacol 85:651-7
Brocato, Jason; Fang, Lei; Chervona, Yana et al. (2014) Arsenic induces polyadenylation of canonical histone mRNA by down-regulating stem-loop-binding protein gene expression. J Biol Chem 289:31751-64
Brocato, Jason; Costa, Max (2013) Basic mechanics of DNA methylation and the unique landscape of the DNA methylome in metal-induced carcinogenesis. Crit Rev Toxicol 43:493-514
Arita, Adriana; Muñoz, Alexandra; Chervona, Yana et al. (2013) Gene expression profiles in peripheral blood mononuclear cells of Chinese nickel refinery workers with high exposures to nickel and control subjects. Cancer Epidemiol Biomarkers Prev 22:261-9
Passantino, Lisa; Muñoz, Alexandra B; Costa, Max (2013) Sodium metavanadate exhibits carcinogenic tendencies in vitro in immortalized human bronchial epithelial cells. Metallomics 5:1357-67

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